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Home , Abscess, Alopecia mucinosa, Folliculitis, Folliculitis decalvans, Fungal folliculitis, Hidradenitis

Acta Clin Croat 2011; 50:395-402 Review

DIFFERENTIAL DIAGNOSIS OF THE SCALP HAIR

Liborija Lugović-Mihić1, Freja Barišić2, Vedrana Bulat1, Marija Buljan1, Mirna Šitum1, Lada Bradić1 and Josip Mihić3

1University Department of Dermatovenereology, 2University Department of , Sestre milosrdnice University Hospital Center, Zagreb; 3Department of , Dr Josip Benčević General Hospital, Slavonski Brod, Croatia

SUMMARY – Scalp hair folliculitis is a relatively common condition in dermatological practice and a major diagnostic and therapeutic challenge due to the lack of exact guidelines. Generally, inflammatory diseases of the pilosebaceous follicle of the scalp most often manifest as folliculitis. There are numerous infective agents that may cause folliculitis, including , and fungi, as well as many noninfective causes. Several noninfectious diseases may present as scalp hair folli- culitis, such as capillitii, capitis abscendens et suffodiens, erosive pustular , lichen planopilaris, eosinophilic pustular folliculitis, etc. The classification of folliculitis is both confusing and controversial. There are many different forms of folliculitis and se- veral classifications. According to the considerable variability of histologic findings, there are three groups of folliculitis: infectious folliculitis, noninfectious folliculitis and perifolliculitis. The diagno- sis of folliculitis occasionally requires histologic confirmation and cannot be based solely on clinical appearance of scalp . This article summarizes prominent variants of inflammatory diseases of the scalp with and appertaining histological features. Key words: Folliculitis; Scalp; Perifolliculitis

Introduction Classification of folliculitis is both confusing and controversial. There are many different forms of fol- Folliculitis is defined as the presence of inflamma- liculitis and several classifications. According to the tory cells within the wall and ostia of the hair fol- considerable variability of histologic findings, there licle, creating a follicular-based pustule. Folliculitis are three groups of folliculitis: infectious folliculitis, frequently manifests on the scalp, face, neck and but- 1 noninfectious folliculitis and perifolliculitis (Table 1). tocks . It can be superficial (ostiofolliculitis) or deep The last one, perifolliculitis, is the process in which (such as furuncle, , etc.). When folliculitis inflammatory cells surround the follicle without pen- lesions are deep, they are usually accompanied by peri- etrating into it. Histologically, there is a chronic peri- follicular , followed by follicular rupture follicular lymphocytic inflammation that clinically (perifolliculitis) and resulting . manifests as the presence of prominent plugs of kera- tin within the dilated follicular orifice. Correspondence to: Liborija Lugović-Mihić, MD, PhD, Universi- Folliculitis is usually characterized by the pres- ty Department of Dermatovenereology, Sestre milosrdnice Uni- ence of perifollicular , , pustules and versity Hospital Center, Vinogradska c. 29, HR-10000 Zagreb, Croatia vesicles that may be perforated by a hair in acute cases, E-mail: [email protected] while chronic-stage lesions present as follicular hyper- Received April 20, 2009, accepted October 15, 2011 keratosis with prominent plugs of within the

Acta Clin Croat, Vol. 50, No. 2, 2011 395 Liborija Lugović-Mihić et al. Differential diagnosis of the scalp hair folliculitis

Table 1. Differential diagnosis of the scalp hair folliculitis according Camacho et al.2

FOLLICULITIS AND PERIFOLLICULITIS

Infections/infestations Noninfectious (folliculitides) Perifolliculitis

Other Superficial Deep Superficial Deep Predominantly possibilities Predominantly (generally (generally (generally (generally lymphocytic (spongiotic granulomatous suppurative) granulomatous) suppurative) granulomatous) folliculitis) Primary Secondary Fungi: Demodicosis vulgaris Acne vulgaris Pruritic Keratosis Demo- Perioral folliculitis of pilaris and dicosis dermatitis Pityrosporum and and perioral Lupoid keratosis Vitamin C dermatitis rosacea spinulosa deficiency Acneiform Acne Fox-Fordyce eruption Bacteria Eosinophilic conglobata disease Keratosis Vitamin A secondary to (Bockhart`s pustular folliculitis Keloidal acne pilaris deficiency ) Majocchi`s of the neck Infundibulo- atrophicans Secondary trichophytic Toxic erythema folliculitis Due to syphilis of the newborn Perforating Lichen lithium folliculitis planopilaris Viruses: Furuncle Follicular Toxicoderma: Pityriasis zoster Carbuncle Mechanical and Halogens rubra pilaris Molluscum chemical traumas Lithium contagiosum Sycosis Toxicodermas: Pseudofolliculitis Acneiform Halogens syphilis Steroids

Pseudofolliculitis follicular orifice1. Inflammatory diseases of the scalp Thus, folliculitis can be classified according to his- hair follicle frequently manifest as folliculitis, which tological features and/or presence of microbiological may lead to cicatricial or non-cicatricial alopecia, de- agents. There are several characteristic histopathologic pending on whether or not the perifollicular infiltrate patterns of hair scalp folliculitis2. In acute folliculitis, or the etiologic agent spares the hair follicle2,3. It is moderate neutrophil infiltrate can be seen infiltrating often difficult to make an adequate diagnosis of scalp follicular epithelium, with the formation of micro- or hair folliculitis and it usually requires considerable macro . Tissue necrosis may be discrete and time and effort to recognize and treat the disease. is usually limited to the follicular infundibulum and Besides the noninfectious causes, there are numer- the adjacent , or it may be significant, affect- ous infective that may cause folliculitis, ing the entire pilosebaceous complex. In chronic fol- including bacteria, viruses and fungi. mel- liculitis there is moderately dense lymphocytic infil- litus, , maceration, tight-fitting clothes, trate, usually a granulomatous infiltrate with a foreign particularly in obese people, inadequate use of topical body reaction around the keratin. The inflammation is and halogenated compounds, care nodular, poorly defined and composed of neutrophils, products and topical hydrocarbons, such as oils or tars , histiocytes, and giant cells. Plasmacytic (occupational exposure) may precipitate exacerbation chronic folliculitis predominantly occurs in facial fol- of folliculitis. In addition, immunocompromised pa- licles, such as , keloidal acne and tients, such as HIV/AIDS patients, may present with solid facial , folliculitis decalvans and carbun- various types of folliculitis. cle2,4.

396 Acta Clin Croat, Vol. 50, No. 3, 2011 Liborija Lugović-Mihić et al. Differential diagnosis of the scalp hair folliculitis

Other histological forms of folliculitis are pre- covered by grayish scales. Hairs break at 4-6 mm and dominantly eosinophilic folliculitides and spongiotic if they are plucked and placed on a black surface, one folliculitides with characteristic features of infundib- can see the surrounding white ‘frosted sheath’ (spores ulofolliculitis. One distinct form is follicular mucino- of the mosaic ectothrix). Hairs fluorescence in Wood’s sis, which often histologically presents in spongiotic light and can therefore be easily identified2. folliculitis as keratinocytes get separated by mucin Trichophytic ringworm tinea of the scalp (black dots deposits, but dermal mucin deposits can also be found tinea) affects only several follicles and manifests with in erythematosus and Fox-Fordyce disease. De- multiple small alopecic areas, which sometimes merge struction of the hair follicle can sometimes ensue, at into a larger polycyclic patch with the characteristic the ‘end-stage’ of folliculitis. Suppurative and granu- interior composed of healthy hair. The most specific lomatous folliculitis generally destroys the follicle sign is the presence of ‘black dots’, which is very fragile leading to cicatricial alopecia. The presence of keratin hair infested by parasite, broken at the level is important as well. Prominent plugs of keratin with- of infundibulum or slightly above. Dermatopatho- in the dilated follicular orifice lead to chronic-stage logical features of tinea tonsurans are chronic der- perifolliculitis. matitis with vasodilatation, lymphocytic perivascular infiltrates with occasional spongiosis. Special staining Folliculitis Due to Infective Agents may reveal the in the corneal layer, ecto- or The majority of infectious folliculitides are caused endothrix arthrospores and Adamson’s fringe. by bacteria and fungi (such as pityrosporum, , Kerion Celsi is an inflammatory tinea of the scalp, or other agents)5-7. These clinical variants of folliculitis generally caused by zoophilic, geophilic or anthropo- can be diagnosed by adequate sampling, swabs, KOH philic dermatophytes, accompanied by severe inflam- examination/or fungal cultures of expressed follicu- matory reaction. It starts as tinea tonsurans and soon lar content. Thereby, diagnosis of these skin changes becomes indurated and covered with squamous crusts includes identification of the , while and pustules. In a few weeks it becomes red, painful includes treatment of the infection. and warm, from small disseminated pustular plaques Viral folliculitis is rare. Folliculitis due to herpes to plaques up to 10 cm. Deep suppurative folliculitis simplex hominis and varicella-zoster may occasionally af- and perifolliculitis occasionally reaching the hypoder- fect the pilosebaceous structures, affecting the beard mis can be seen on histopathologic examination. Over area in males (‘viral sycosis’), manifesting as a group of time, the infiltrate becomes lymphocytic. erythematous papulovesicles or umbilicated vesicles. Favus is folliculitis caused by T. schoenleinii and it is currently prevalent in Spain. It begins with small erythematosquamous patches with slight infiltration. Dermatophytes, saprophytes such as Pityrospo- Underneath the scales, there are pseudopustular yel- rum and Candida sp. may cause various folliculitides. lowish elements in the initial phase of the ‘scutulum’ Dermatophytic folliculitis is very common and can be of the ‘favic cup’, somewhat elevated and umbilicated caused by all dermatophytes except for E. floccosum, T. centrally, sulfur yellow in color with soil-like consis- concentricum and M. persicolor. In vitro cultures can be tency, since they are made up of mycelia and epithelial used for identification of these keratinophilic fungi. detritus. The underlying is emanating rather We can therefore visualize whether the hair is invaded unpleasant odor caused by detritus, , and by concentric destruction, or by perforation with ‘per- secondary bacterial infection. Affected hair is luster- forating organs’, indicating T. mentagrophytes. There less, gray, dry, and fluorescent under Wood’s light. is variation in clinical presentation of dermatophytic Pityrosporum folliculitis may be seen on the skin in folliculitis. periphery of the scalp. This is a superficial pustulosis Microsporous ringworm tinea of the scalp (great which most frequently affects the back and the upper gray patch tinea) is a non-inflammatory tinea ton- part of the thorax, typical sites for Pityrosporum or- surans of the scalp characterized by typical large biculare, although it can sometimes affect upper limbs round or polycyclic plaques and small satellite patches as well.

Acta Clin Croat, Vol. 50, No. 3, 2011 397 Liborija Lugović-Mihić et al. Differential diagnosis of the scalp hair folliculitis

Folliculitis due to Candida manifests with occa- Noninfectious Types of Folliculitis sionally painful papules, nodules and pustules in hairy Folliculitis decalvans capillitii (folliculitis spinulosa areas, especially on the scalp and the beard. decalvans) is a scarring folliculitis of the scalp that leads to alopecia1,4. The nature of folliculitis decalvans Bacterial Folliculitis is unclear, but S. aureus is frequently isolated from the Bacterial folliculitis can be superficial or deep, culture11. It primarily affects adult men, often immu- most often caused by aureus, streptococ- nosuppressed patients, either with diabetes mellitus, 1,2 cus, proteus, pseudomonas or coliform bacilli . Predis- chronic renal disease, gammopathy or iatrogenic im- posing factors include hyperhidrosis, occlusion, mac- munosuppression. The inflamed follicles coalesce, eration, traction depilation, topical corticosteroids and progressing in depth and laterally, forming follicular exposure to oils or other chemical substances, or can papulopustules, slightly pruriginous, causing several result from an ‘erosive pustular dermatosis’ due to S. small patches of cicatricial alopecia with follicular fi- aureus in a patient that underwent scalp operation. brosis. The skin becomes atrophic, resembling pseu- Superficial folliculitis (‘osteofolliculitis’) is an in- dopelade, while at the periphery follicular pustules fection of the follicular ostium, which manifests with continue to form1,12. The disease is chronic and dif- painful erythematopapular perifollicular lesions. In ficult to stop. The acute stage of folliculitis decalvans localized forms it usually starts with small white-yel- capillitii resembles highly inflammatory , low pustules located in follicular orifices surrounded while the scarring stage mimics all other types of scar- by erythema. It usually manifests on the upper lip in ring alopecia, including discoid lupus erythematosus children, whereby staphylococcus can originate from and . Histopathologically, early lesions nearby nasal fossae, or can disseminate through the are marked by neutrophilic folliculitis and frank ab- beard and other hairy areas like the scalp, and spread scesses within the follicles, while nonspecific scarring due to scratching8. alopecia ensues later. Neutrophilic follicular abscess Deep folliculitis close to the scalp and on the scalp can be seen around the follicles and sweat glands, manifests with sycosis, furuncle, carbuncle, etc. When which rapidly leads to a granulomatous infiltrate with the folliculitis extends beyond the infundibulum, it a large number of plasma cells2. results in both superficial and deep abscess. As deep The disease is resistant to therapy but beneficial -ef abscess does not reach the bulb, usually there is no fects of (600 mg/day/7 weeks) and oral fu- residual alopecia. There are several types of deep folli- sidic acid (1.5 mg/day/3 weeks or topical 1.5% cream) culitis, such as furuncle, a deep and necrotizing acute with the addition of zinc sulfate (400 mg/day/6 weeks)2 folliculitis, manifesting as an inflammatory nodule have been reported. Dapsone (100-150 mg/day/sev- with central pus produced by bacterial hair follicle in- eral months) is worth trying. Therapy with systemic fection1. It is usually located on the face, neck, perine- , based on culture results, shows only tran- um, breasts, axillae, gluteal region and thighs. Car- sient effect and is often disappointing. In severe cases, buncle is an accumulation of furuncles with marked short courses of systemic corticosteroids are indicated inflammation and granuloma1. It is more often seen to reduce inflammation. Topical antibacterial therapy in immunocompromised people and in chronic pro- brings little relief, e.g., lotions or solutions contain- cesses. Clinically, there is a swelling containing a ing antibiotics such as , often combined large number of pustules, which rapidly open up on with topical corticosteroids1. multiple sites, with exudation of necrotic tissue and Folliculitis sclerotisans nuchae (keloidal folliculitis), pus through these openings, lasting for several days a scarring form of chronic folliculitis that manifests as and leaving a deep scar behind. follicular-based papules and pustules that eventually Syphilitic folliculitis is a rare manifestation of sec- result in -like . It is mostly located on the ondary syphilis, which may appear in the frontal hair neck, and mainly occurs in dark skinned people and implantation line and nasogenian folds in the second- Caucasians, especially in association with seborrheic ary-tertiary phase, its progression resulting in grouped dermatitis and sometimes with alopecia. Histological linear or polycyclic arranged elements9,10. features include dense lymphoplasmacytic inflamma-

398 Acta Clin Croat, Vol. 50, No. 3, 2011 Liborija Lugović-Mihić et al. Differential diagnosis of the scalp hair folliculitis tory infiltrates around thick, compact, keloidal col- oid scars, predominantly located on the face, throat, lagen bands, which correspond to destroyed follicles shoulders, chest, back, gluteal region, or beside scalp or sometimes peripilar . Therapy includes area. In the areas with apocrine glands, like the axil- topical steroids, antibiotics, retinoids, cryotherapy, e lae and the groin, this causes suppurativa tc. or dissecting in the scalp region. Histologic Tufted hair folliculitis manifests with a ‘tuft’ of examination shows deep folliculitis, progressing to- hair made up of 5 to 20 hairs, which appear normal wards the formation of abscesses and, with subse- in the follicular openings that remain in the alopecic quent reepithelialization of the follicular unit, leaving plaque13. It also appears to be caused by S. aureus, a sinus and fibrosis. , dissect- although it is possibly related to immunodeficient ing cellulitis and often coexist as a states or is of ‘nevoid origin’. It manifests as exudative follicular occlusion triad. patches on the parietal or occipital areas, which tend Acne necrotica (acne varioliformis, necrotizing to progress peripherally leaving cicatricial alopecia in lymphocytic folliculitis) is a rare, chronic pruritic the center. Histologically, there is a perifollicular in- eruption of multiple follicular papules which rapidly filtrate composed of lymphocytes, eosinophils, plas- progress into umbilicated vesiculo-papules or pus- mocytes and neutrophils with inflammation around tules, sometimes with a central crust, mostly located the upper portion of the follicle, which does not affect in the temporal areas, nape and the frontal implan- the bulb. Topical antiseptics and systemic antibiotics tation line2. Most patients are adult women. Over (erythromycin, and ) improve weeks, it slowly involutes, leaving a varioliform scar1. the inflammatory component. Use of shampoos with Histopathologically, there is epidermal damage with mineral oils and keratolytics is also advised. mixed dermal inflammatory infiltrates in more- ad Erosive pustular dermatitis is a pustular dermatosis vanced crusted lesions, while lymphocytic perifolli- with erosions and crusts covering the scalp, generally cular infiltrates and other adnexal structures in early caused by S. aureus, or rarely S. epidermidis, Pseudomo- lesions sometimes cause spongiosis. Excoriated bacte- nas aeruginosa, coagulase negative staphylococcus, rial folliculitis or rarely herpes simplex is con- diphtheroids, coliforms and Proteus mirabilis. Candida sidered in its etiopathogenesis. Isotretinoin has good sp. and other fungi have also been cultured in some therapeutic results and corticosteroids often bring cases, but these seem to reflect secondary coloniza- immediate improvement. Topical therapy is generally tion14,15. Follow-up is very important since carcinoma- ineffective, although potent topical corticosteroids or tous transformation may occasionally occur. Despite benzoyl peroxide may be helpful1. the nonspecific histological features, there is chronic Acneiform eruptions can sometimes be seen on perifollicular inflammatory infiltrate composed of the scalp, such as in case of . Chloracne are lymphocytes, plasmocytes and giant cells15. It has been caused by the exposure to chlorinated compounds suggested that exposure to ultraviolet light may be a which can be found in industry, usually in electrical predisposing factor. Treatment includes nonsteroid conductors, and therefore may represent an occupa- anti-inflammatory agents, topical and systemic antibi- tional disease. Clinically, it manifests with and otics. Superficial bacterial folliculitis usually responds comedones that are usually open, covering temporal well to antiseptic baths such as povidone iodide and areas, cheeks, throat and retroauricular region16. The chlorhexidine gluconate, to astringent aluminum sub- treatment includes topical/oral antibiotics, topical/ acetate compresses and to topical antibiotics (poly- oral retinoids excision, laser ablation, and drug with- myxin B sulfate, neomycin sulfate, fusidic acid and drawal. ). Deep folliculitis requires treatment with Lichen planopilaris is a form of lichen planus locat- systemic antibiotics (e.g., , azithromy- ed on the scalp, characterized by perifollicular erythe- cin, semisynthetic ). ma and small keratotic pruriginous follicular papules Acne conglobata represent a chronic inflammatory resulting in small alopecic plaques17-19. It is more com- process which manifests with nodules, cysts, abscess- mon in the hair implantation line, both the frontal es, draining sinus tracts, comedones and multiple kel- hair implantation line and the occipital line, although

Acta Clin Croat, Vol. 50, No. 3, 2011 399 Liborija Lugović-Mihić et al. Differential diagnosis of the scalp hair folliculitis it can also appear on any other part of the scalp. The lar plugs on the nose and cheeks, which later expand disease occurs more frequently in women between to the scalp, neck and extremities causing atrophy in age 30 and 602. There are three different types of these areas. The atrophic aspect of the cheeks and ci- the disease according to clinical manifestations and catricial alopecia on the scalp, eyebrows and eyelashes histopathologic features: keratotic follicular papules make all these children look very much alike. At the and inflammatory lichenoid infiltration in the folli- beginning, it is accompanied with cysts on cular epithelium; violaceous or erythematous plaques, the cheeks, or possible atopy, corneal opacities, pho- some with follicular prominence and an inflammatory tophobia, conjunctivitis, keratitis, blepharitis and pal- lichenoid infiltrate and follicular papules associated moplantar hyperkeratosis. Oral retinoids have been with perifollicular and interfollicular inflammatory reported to lead to improvement. infiltrate resulting in fibrosing alopecia2. Eosinophilic pustular folliculitis (Ofuji’s syndrome) Rarely, patchy cicatricial alopecia of the scalp is as- is a rare dermatosis of unknown etiology, character- sociated with non-scarring alopecia of the axillary and ized by recurrent episodes of eruptive sterile follicular pubic areas, and grouped spinous follicular papules re- papulopustules in seborrheic areas, accompanied by sembling on the trunk and extremi- and eosinophilia. It is most common in ties (Piccardi-Lassueur-Graham-Little syndrome). men and the general population in the third decade of Pityriasis rubra piliaris is characterized by multiple life, in which the papulopustules tend to form round follicular papules, sometimes with a central black cor- ring-shaped or polycyclic plaques with peripheral pro- neal plug, which generally accompanies or precedes gression and central clearing, with residual scaling and seborrheic dermatitis of the scalp20,21. This disease pigmentations. The histopathologic features include manifests with a yellow-orange erythematosquamous infundibular follicular pustules mainly composed of plaques, often developing on the scalp, with obvious eosinophils and polynuclears. Topical corticosteroids islands of sparring and palmoplantar hyperkeratosis. or tacrolimus ointment can be prescribed. Clinically it shows multiple follicular papules with Follicular mucinosis () on the scalp a central corneal plug on the lateral surfaces of the is characterized by the presence of follicular papules thighs and arms, gluteal region and forearms. There and indurated plaques associated with alopecia. The is a corneal plug which occludes the pore and dilates disease is accompanied with fungoides and the follicular ostium, hyperkeratosis, dermal vasodi- angiolymphoid hyperplasia with eosinophilia, less fre- latation with chronic perivascular and periadnexal in- quently with chronic discoid lupus erythematosus and flammatory infiltrate. Therapy may include systemic Goodpasture’s syndrome. There is another form of retinoids, topical corticosteroids and retinoids, mild idiopathic or primary origin (mainly affects children keratolytic agents, etc. and young adults) presenting by grouped follicular Keratosis pilaris atrophicans is characterized by papules. They show a tendency to coalesce into more different clinical presentations which may be classi- or less well defined erythematous plaques with dilated fied in two groups: hair keratosis and pseudopelade. follicular orifices on the surface of these plaques, as There are hair keratoses that cause atrophy in glabrous well as alopecia. skin of the face, such as folliculitis atrophicans faciei Follicular is characterized by the and atrophoderma vermiculatum; however, keratosis presence of infiltrated follicular papules located on the follicularis spinulosa decalvans should be referred as face, neck, trunk and extremities, and sometimes on pseudopelade or ‘scarring follicular keratosis’2,22. The the scalp25. Histopathologically, there are perifollicu- difference between keratosis pilaris and these four der- lar and intrafollicular infiltrates of atypical lympho- matoses is the greater inflammatory component seen cytes with convoluted nuclei. One must differentiate in the latter, as well as intense clinical erythema23. this disease from follicular lymphomatoid papulosis, Keratosis follicularis spinulosa decalvans, a type of especially type B or lymphocytic papulosis. It should X-linked recessive genodermatosis, causes cicatricial be treated with nitrogen mustards and/or electron alopecia of the scalp and eyebrows during infancy or therapy, but also with topical corticosteroids, photo- adolescence2,24. It begins with corneal filiform follicu- therapy, etc.

400 Acta Clin Croat, Vol. 50, No. 3, 2011 Liborija Lugović-Mihić et al. Differential diagnosis of the scalp hair folliculitis

Perifolliculitis cal practice. However, only such adequate diagnostic procedures result in correct diagnosis and successful The prominent disease in this group is perifollicu- therapeutic outcomes. litis capitis abscendens et suffodiens, but, according to some authors, in this group keratosis piliaris atro- phicans, lichen planopilaris, , References 2 perioral dermatitis, etc. are also included . 1. Braun-Falco O, Plewig G, Wolf HH, Burg- Perifolliculitis capitis abscendens et suffodiens is a dorf WHC, editors. . 2nd completely revised severe destructive folliculitis with sinus tracts and fis- edition. Berlin: Springer-Verlag, 2000. tulae leading to scarring alopecia, and is often part of 2. Camacho F. Cicatricial alopecias. In: Camacho F, the acne inversa spectrum1. It occurs almost exclusively Montagna W, editors. Trichology – disease of the pi- in young men and may be more common in the black losebaceous follicle. Madrid: Libros Princeps, Aula Medica population. The cause is unknown, but is often associ- Library, 1997:537-51. ated with recurrent gram-negative . Lesions 3. Ross EK, Tan E, Shapiro J. Update on primary cicatri- cial alopecias. J Am Acad Dermatol 2005;53:38-40. begin as multiple, firm scalp nodules that rapidly de- velop into fluctuant ridges that eventually discharge 4. Abeck D, Korting HC, Braun-Falco O. Folli- 1 culitis decalvans. Long-lasting response to combined therapy purulent material leading to . The folliculitis with fusidic acid and zinc. Acta Derm Venereol (Stockh) manifests on the scalp or nape leading to persistent 1992;72:143-5. inflammation and destruction of follicles. The skin 5. Camacho F. Dermatosis zooparasitarias. In: Armijo may be covered with crusts and scales; pressure on M, editor. Plan de perfeccionamiento en dermatología. Der- one fluctuant area may result in multiple follicular matosis por agentes vivos. Madrid: Editorial Médica Interna- openings26,27. Flares are very frequent and the disease cional Ed., 1990:301-7. is chronic. Histopathologic features reveal moderately 6. Karincaoglu Y, Esrefoglu Seyhan M, Bay- dense, perifollicular lymphocytic inflammation affect- ram N, Aycan O, Taskapan H. Incidence of Demod- ex folliculorum in patients with end stage chronic renal failure. ing the lower half of the dermis and extending down Ren Fail 2005;27:495-9. into the subcutaneous fat, necrosis and scarring. Smear rd 7. Sanfilippo AM, English JC 3 . Resistant scalp folli- of pustular content is useful, and often a wide variety culitis secondary to Demodex infestation. Cutis 2005;76:321-4. of organisms can be found, frequently gram-negative 8. Camacho F. Enfermedades fitoparasitarias. In: Du- bacteria prevail. The disease is extremely difficult to lanto F, Armijo M, Aly R, Levit S, editors. The treat, e.g., broad-spectrum antibiotics, systemic cor- changing spectrum of streptococcal and staphylococcal dis- ticosteroids (40-60 mg/day/tapered over 3 weeks), or ease. Curr Opin Dermatol 1993;1:290-5. 1,28 isotretinoin (1 mg/kg /day/12-20 weeks) may help . 9. Camacho F. Dermatosis genitals no venéreas. In: Perea Topical therapy includes disinfectant solutions such E, editor. Enfermedades de transmisión sexual. Barcelona: as chinosol. Epilation of involved follicles may reduce Doyma Ed., 1993:125-45. inflammation and its spread. When the inflammatory 10. Cuozzo DW, Benson PM, Sperling LC, Skel- process resolves, surgical excision of scarred areas is ton III HG. Essential syphilitic alopecia revisited. J Am Acad Dermatol 1995;32:840-4. recommended1. 11. Otberg N, Kang H, Alzolibani AA, Shapiro J. Folliculitis decalvans. Dermatol Ther 2008;21:238-44. Conclusion 12. Moreno JC. Pseudopelada de Brocq. Cuadros pseudope- ládicos. Alopecias en dermatosis especiales. Monogr Derma- Differential diagnosis of scalp hair folliculitis is tol 1990;3:157-64. broad. It is crucial to recognize and exclude an in- 13. Luelmo-Aguilar J, González-Castro U, fectious diseases and to confirm clinical diagnosis Castells-Rodellas A. Tufted hair folliculitis. A by histopathologic analysis. Repeated swabs, KOH study of four cases. Br J Dermatol 1993;128:454-7. examination/or fungal cultures and tissue sampling 14. Layton AM, Cunliffe WJ. Erosive pustular dermatosis for histopathologic analysis are often necessary to of the scalp following . Br J Dermatol 1995;132:472-3. confirm the diagnosis of scalp hair folliculitis, which 15. Caputo R, Verladi S. Erosive pustular dermatosis of can represent a significant burden to everyday clini- the scalp. J Am Acad Dermatol 1993;28:96-8.

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16. Rodríguez-Pichardo A, Camacho F. Chlo- 22. Baden HP, Byers HR. Clinical findings, cutaneous pa- racne as a consequence of a family accident with chlorinated thology, and response to therapy in 21 patients with keratosis dioxins. J Am Acad Dermatol 1990;22:1121. pilaris atrophicans. Arch Dermatol 1994;130:469-75. 17. Matta M, Kibbi A-G, Khattar J, Salman SM, 23. Oranje AP, Van Osch LDM, Oosterwijk JC. Zaynoun ST. Lichen planopilaris: a clinicopathologic Keratosis pilaris atrophicans. One heterogeneous disease study. J Am Acad Dermatol 1990;22:594-8. or a symptom in different clinical entities? Arch Dermatol 18. Mehregan DA, Van Hale HM, Muller SA. Li- 1994;130:500-2. chen planopilaris: clinical and pathologic study of forty-five 24. Puppin D, Aractingi S, Dubertret L, patients. J Am Acad Dermatol 1992;27:935-42. Blanchet-Bardon C. Keratosis follicularis spinulosa 19. Oremović L, Lugović L, Vučić M, Buljan M, decalvans: report of a case with ultrastructural study and un- Ožanić-Bulić S. Cicatricial alopecia as a manifestation successful trial of retinoids. Dermatology 1992;184:133-6. of different dermatoses. Acta Dermatovenerol 2006;14:245- 25. Pereyo NG, Requena L, Galloway J, 52. Sangűeza OP. Follicular mycosis fungoides: a clinicohis- 20. Clayton BD, Jorizzo JL, Hitchcock MG, topathologic study. J Am Acad Dermatol 1997;36:563-8. Fleischer AB, Williford PM, Feldman SR, 26. Khumalo NP, Jessop S, Gumedze F, Ehrlich White WL. Adult pityriasis rubra pilaris: a 10-year case R. Hairdressing and the of scalp disease in Afri- series. J Am Acad Dermatol 1997;36:959-64. can adults. Br J Dermatol 2007;157:981-8. 21. Drago F, Maietta G, Parodi A, Rebora A. Ker- 27. Ogunbiyi A, George A. Acne keloidalis in females: atosis pilaris decalvans non-atrophicans. Clin Exp Dermatol case report and review of literature. J Natl Med Assoc 1993;18:45-46. 2005;97:736-8. 28. Parish LC, Witkowski JA, Mirensky Y. Recent advances in antimicrobial therapy of bacterial infections of the skin. Curr Opin Dermatol 1993;1:263-70.

Sažetak

DIFERENCIJALNA DIJAGNOZA FOLIKULITISA VLASIŠTA

L. Lugović-Mihić, F. Barišić, V. Bulat, M. Buljan, M. Šitum, L. Bradić i J. Mihić

Folikulitis vlasišta je relativno česta pojava u dermatološkoj praksi koja zbog nedostatka jasnih smjernica predstavlja značajan dijagnostički i terapijski izazov. Općenito se upalne bolesti pilosebacealnog folikula u vlasištu najčešće manife- stiraju kao folikulitis. Postoje brojni infektivni agensi koji mogu uzrokovati folikulitis vlasišta, kao što su bakterije, virusi i gljive, kao i mnogi neinfektivni uzroci. Nekoliko neinfektivnih bolesti mogu imati sliku folikulitisa u vlasištu, kao što su folliculitis decalvans capillitii, perifolliculitis capitis abscendens et suffodiens, erozivni pustularni dermatitis, lichen planopilaris, eozinofilni pustularni folikulitis i drugo. Klasifikacija folikulitisa također je nejasna i kontroverzna. Tako se navode različiti oblici folikulitisa i nekoliko njihovih klasifikacija. Prema ključnim varijacijama histoloških nalaza postoje tri skupine folikulitisa: infektivni folikulitis, neinfektivni folikulitis i perifolikulitis. Dijagnoza folikulitisa povremeno zahtijeva histološku potvrdu i ne može se osnivati samo na kliničkoj pojavi lezija vlasišta. U ovom članku su obuhvaćene moguće upalne bolesti folikula vlasišta s mogućim diferencijalnim dijagnozama i pripadajućim histološkim značajkama. Ključne riječi: Folikulitis; Koža glave; Perifolikulitis

402 Acta Clin Croat, Vol. 50, No. 3, 2011